Rheumatoid Arthritis (cont.)

William C. Shiel Jr., MD, FACP, FACR

Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.

Melissa Conrad Stöppler, MD

Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.

Catherine Burt Driver, MD

Catherine Burt Driver, MD, is board certified in internal medicine and rheumatology by the American Board of Internal Medicine. Dr. Driver is a member of the American College of Rheumatology. She currently is in active practice in the field of rheumatology in Mission Viejo, Calif., where she is a partner in Mission Internal Medical Group.

Is it possible to prevent rheumatoid arthritis?

Currently, there is no specific prevention of rheumatoid arthritis. Because cigarette smoking, exposure to silica mineral, and chronic periodontal disease all increase the risk for rheumatoid arthritis, these conditions should be avoided.

What research is being done on rheumatoid arthritis?

Scientists throughout the world are studying many promising areas of new treatment approaches for rheumatoid arthritis. Indeed, treatment guidelines are evolving with the availability of newer treatments. These areas include treatments that block the action of the special inflammation factors, such as tumor necrosis factor (TNF alpha), B-cell and T-cell function, as well as interleukin-1 (IL-1), as described above. Many other drugs are being developed that act against certain critical white blood cells and chemical messengers involved in rheumatoid inflammation. Also, new NSAIDs with mechanisms of action that are different from current drugs are on the horizon.

Better methods of more accurately defining which patients are more likely to develop more aggressive disease are becoming available. Recent antibody research has found that the presence of citrulline antibodies in the blood (see above, in diagnosis) has been associated with a greater tendency toward more destructive forms of rheumatoid arthritis.

Studies involving various types of the connective tissue collagen are in progress and show encouraging signs of reducing rheumatoid disease activity. Finally, genetic research and engineering are likely to bring forth many new avenues for earlier diagnosis and accurate treatment in the near future. Gene profiling, also known as gene array analysis, is being identified as a helpful method of defining which people will respond to which medications. Studies are under way that are using gene array analysis to determine which patients will be at more risk for more aggressive disease. This is all occurring because of improvements in technology. We are at the threshold of tremendous improvements in the way rheumatoid arthritis is managed.